Overview of renal damage in multiple myeloma
Renal damage in multiple myeloma, also known as myeloma tubular nephropathy, refers to the infiltration of myeloma cells, as well as the production of large quantities of abnormal immunoglobulins excreted from the kidneys, resulting in renal lesions. Clinically, it is mainly seen that the infiltration of abnormal plasma cells (i.e., myeloma cells) destroys bones, causing bone disease and hypercalcemic anemia. About 2/3 of the patients develop proteinuria during the course of the disease, and about half of the patients are accompanied by renal insufficiency, and renal function is one of the most important factors determining the prognosis. Treatment in addition to multiple myeloma chemotherapeutic drug combination program, should be actively control infection, for renal damage related factors for rational treatment.
Etiology
The etiology of MM is not known. It may be related to genetic factors, viral infection, ionizing radiation, chronic antigenic stimulation and other factors. In recent years, it has been found that C-myc gene recombination, some of which have high levels of H-ras gene protein products, and abnormal regulation of lymphokine, especially interleukin-6 secretion, are related to the development of MM.
The factors of myeloma kidney damage are: ① Nephrotoxic effect of light chain protein. ② Hypercalcemia. ③ Hyperuricemia nephropathy. ④ Renal amyloidosis. ⑤ Hyperviscosity. ⑥ Pyelonephritis. ⑦ Acute renal failure induced by dehydration drugs and contrast media. ⑧ Lymphoid plasma cell infiltration of renal tissue.
Symptoms
Typical multiple myeloma (MM) mainly has bone pain, anemia and bleeding tendency, fever, renal insufficiency and other manifestations, but also can be seen widespread osteoporosis, increased globulin, recurrent infections, etc. In addition, there may be hypercalcemia symptoms, hyperviscosity syndrome, neuropathy and amyloidosis manifestations. Patients often go to orthopedics or rehabilitation department due to bone pain, which is often misdiagnosed as tuberculosis, osteoarthrosis and lumbar strain. Kidney injury manifestations: hematuria, proteinuria, foamy urine, nephrotic syndrome, chronic tubular insufficiency, chronic renal failure, acute renal failure, urinary tract infection.
Examination
1. Blood test
Blood routine, liver and kidney function, immunoglobulin measurement, serum immunoelectrophoresis, etc.
2. Urine examination
Urine routine, 24-hour urine light chain quantification, urine immunofixation electrophoresis, etc.
3.Others
Bone marrow aspiration, bone marrow biopsy, X-ray film, etc.
Diagnosis
Initial screening is usually carried out through simple blood and urine tests to clarify or exclude the diagnosis of multiple myeloma. In some cases, the diagnosis can be confirmed after further tests such as bone marrow aspiration, bone marrow biopsy and X-ray film.
1. Main diagnostic basis of MM
(1) Serum protein electrophoresis: abnormal M protein peaks can be seen between β and γ, or urine light chain protein is persistently positive, accompanied by any of the following: ① bone marrow plasma cells more than 15%, and exclude reactive plasmacytosis caused by chronic infections and connective tissue diseases. ② Positive tissue biopsy. (iii) Osteolytic damage foci, excluding cancer bone metastasis and hyperparathyroidism.
(2) Bone marrow smear: plasma cells more than 10%, primary and juvenile plasma cells or plasma cell count more than 30%.
(3) Acetate fiber film electrophoresis: no abnormal immunoglobulin in serum, no light chain protein detected in urine, but there are osteolytic lesions or tumors accompanied by any one of the following manifestations: ① Bone marrow smear: the number of plasma cells is more than 20%, and other diseases causing plasma cell hyperplasia can be excluded. ② mass biopsy: plasma cell infiltration.
2. Diagnostic basis of multiple myeloma kidney damage
On the basis of MM, renal function abnormalities such as increased globulin, hematuria, proteinuria and foamy urine can be diagnosed.
Treatment
There are two aspects in the treatment of renal damage complicated by MM, one is to reduce the number of myeloma cells and their M protein production, which can be done by systemic chemotherapy, radiotherapy, bone marrow transplantation, blood purification, etc.; the other is systemic supportive therapy and its prevention and treatment of triggering factors.
1. Drinking more water, maintaining sufficient urine output
Light chain proteinuria, hyperviscosity, hypercalcemia and hyperuricemia are often present in this disease, which can cause and aggravate renal damage. Drinking large amounts of water is conducive to the excretion of light chain protein, uric acid and calcium salts, and prevents the formation of tubular patterns in the renal tubules. The amount of water intake during and after chemotherapy or radiotherapy should be more.
2. Prevention and treatment of uric acid nephropathy
Take allopurinol in hyperuricemia, especially in the beginning months of chemotherapy. Alkalizing the urine can reduce the deposition of uric acid and light chain protein in the kidney and the formation of tubular pattern.
3. Prevention and treatment of hypercalcemia
Hypercalcemia can cause renal damage, and nephrotoxicity is enhanced when co-existing with light chain protein. An acute increase in blood calcium above 3.2 mmol/L (13 mg/dL) carries the risk of hypercalcemia crisis and should be corrected promptly.
4. Plasma replacement
For hyperviscosity syndrome caused by large amount of immunoglobulin secreted by the tumor, plasma exchange therapy should be performed.
5. Replacement therapy
More than half of the patients with this disease can develop renal failure, and some patients can be complicated with persistent hypercalcemia, which requires dialysis treatment. Whether hemodialysis or peritoneal dialysis can make the patient turn to safety quickly, and can buy time for chemotherapy.
Prognosis
The prognosis for multiple myeloma nephropathy is a median survival of 6 months in untreated patients and 3 years after chemotherapy. With combination therapy the median survival can be 5 to 10 years or even longer. Survival is related to age, type, stage, and treatment.